<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Welters C</submitter><funding>Deutsche Forschungsgemeinschaft</funding><funding>European Research Council</funding><funding>Deutschen Konsortium für Translationale Krebsforschung</funding><funding>European Union ERC Advanced Grant</funding><funding>Deutsche Krebshilfe</funding><funding>Berliner Krebsgesellschaft e.V.</funding><pagination>1407-1419</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9627264</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>10(11)</volume><pubmed_abstract>Multiple myeloma is a hematologic malignancy of monoclonal plasma cells that accumulate in the bone marrow. Despite their clinical and pathophysiologic relevance, the roles of bone marrow-infiltrating T cells in treatment-naïve patients are incompletely understood. We investigated whether clonally expanded T cells (i) were detectable in multiple myeloma bone marrow, (ii) showed characteristic immune phenotypes, and (iii) whether dominant clones recognized antigens selectively presented on multiple myeloma cells. Single-cell index sorting and T-cell receptor (TCR) αβ sequencing of bone marrow T cells from 13 treatment-naïve patients showed dominant clonal expansion within CD8+ cytolytic effector compartments, and only a minority of expanded T-cell clones expressed the classic immune-checkpo</pubmed_abstract><journal>Cancer immunology research</journal><pubmed_title>Immune Phenotypes and Target Antigens of Clonally Expanded Bone Marrow T Cells in Treatment-Naive Multiple Myeloma.</pubmed_title><pmcid>PMC9627264</pmcid><funding_grant_id>390857198</funding_grant_id><funding_grant_id>882963</funding_grant_id><funding_grant_id>PE 3127/1-1</funding_grant_id><funding_grant_id>HAFF202013 MM</funding_grant_id><funding_grant_id>70113355</funding_grant_id><pubmed_authors>Blanc E</pubmed_authors><pubmed_authors>Rahn HP</pubmed_authors><pubmed_authors>Welters C</pubmed_authors><pubmed_authors>Dornmair K</pubmed_authors><pubmed_authors>Moosmann A</pubmed_authors><pubmed_authors>Strobel J</pubmed_authors><pubmed_authors>Bullinger L</pubmed_authors><pubmed_authors>Hackstein H</pubmed_authors><pubmed_authors>Penter L</pubmed_authors><pubmed_authors>Hansmann L</pubmed_authors><pubmed_authors>Gerbitz A</pubmed_authors><pubmed_authors>Beule D</pubmed_authors><pubmed_authors>Buccitelli C</pubmed_authors><pubmed_authors>Dietze K</pubmed_authors><pubmed_authors>Hsu MT</pubmed_authors><pubmed_authors>Popp O</pubmed_authors><pubmed_authors>Ben Hamza A</pubmed_authors><pubmed_authors>Chen X</pubmed_authors><pubmed_authors>Mertins P</pubmed_authors><pubmed_authors>Blankenstein T</pubmed_authors><pubmed_authors>Stein CA</pubmed_authors><pubmed_authors>Lammoglia Cobo MF</pubmed_authors></additional><is_claimable>false</is_claimable><name>Immune Phenotypes and Target Antigens of Clonally Expanded Bone Marrow T Cells in Treatment-Naive Multiple Myeloma.</name><description>Multiple myeloma is a hematologic malignancy of monoclonal plasma cells that accumulate in the bone marrow. Despite their clinical and pathophysiologic relevance, the roles of bone marrow-infiltrating T cells in treatment-naïve patients are incompletely understood. We investigated whether clonally expanded T cells (i) were detectable in multiple myeloma bone marrow, (ii) showed characteristic immune phenotypes, and (iii) whether dominant clones recognized antigens selectively presented on multiple myeloma cells. Single-cell index sorting and T-cell receptor (TCR) αβ sequencing of bone marrow T cells from 13 treatment-naïve patients showed dominant clonal expansion within CD8+ cytolytic effector compartments, and only a minority of expanded T-cell clones expressed the classic immune-checkpo</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Nov</publication><modification>2026-05-28T03:42:58.267Z</modification><creation>2025-04-04T20:22:18.924Z</creation></dates><accession>S-EPMC9627264</accession><cross_references><pubmed>36122410</pubmed><doi>10.1158/2326-6066.CIR-22-0434</doi></cross_references></HashMap>